The goals of this study are to prospectively explore the relationships of endogenous sex steroid hormones and obesity, and their interactions with lipoprotein cholesterol and apolipoprotein (lipo/apo) levels in 9 and 10 year old black and white adolescent females longitudinally for five years during puberty. There is growing evidence that androgens, particularly when elevated, have an unfavorable effect on lipo/apo levels, tending to lower HDL cholesterol (HDLC) and raise LDL cholesterol (LDLC). Previous studies have confirmed that although pre-pubertal boys and girls have similar lipo/apo levels, post-pubertal boys have a higher ratio of LDLC/HDLC than girls, in part because of their androgen levels. Such lipo/apo levels have been associated with an increased risk of coronary heart disease (CHD). There is also evidence that obese girls tend to be hyperandrogenic and thus may have unfavorable lipo/apo levels and a higher risk of CHD. One of the specific aims of this study is to elucidate whether high androgens precede or are a consequence of obesity. It has also been observed that after puberty there are a significantly larger number of obese black compared to white females. These girls have a higher risk for CHD. We wish to test the hypothesis that the observed increased risk of CHD in black girls associated with obesity may be mediated by a sex steroid hormone modulating effect on lipo/apo levels. This study will examine 700 black and 700 white females in the Cincinnati, Ohio and Washington, DC public and parochial schools as part of a five-year project entitled "Development of Obesity in Young Black and White Females - Clinical Sites" which has been funded by the National Growth and Health Study (NGHS) (NHLBI #HC-55025). As part of the NGHS study, participants will receive a careful physical examinations with attention to pubertal staging and anthopometric measurements including weight, stature and skinfold thickness. Along with NGHS blood samples, additional blood will be obtained in years 1, 3, and 5 for measurement of lipids, lipoprotein cholesterols and apolipoproteins (A1, A2, and B) and sex steroid hormones including plasma total and free testosterone, dehydroepiandrosterone sulfate, estradiol and testosterone estrogen binding globulin. The ultimate goals are to ascertain the role of sex steroid hormones, obesity, and their interactions in determining apo/lipo levels to facilitate pediatric primary prevention of CHD.